Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText.
Kick-your-searchterm to multiple Engines kick-your-query now !>
A dictionary by aggregated review articles of nephrology, medicine and the life sciences
Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

suck abstract from ncbi


10.1007/s00401-017-1709-7

http://scihub22266oqcxt.onion/10.1007/s00401-017-1709-7
suck pdf from google scholar
C5508034!5508034 !28401333
unlimited free pdf from europmc28401333
    free
PDF from PMC    free
html from PMC    free

suck abstract from ncbi


Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534

Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534

Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534

Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28401333 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117
pmid28401333
      Acta+Neuropathol 2017 ; 134 (2 ): 187-205
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • Interactions of pathological proteins in neurodegenerative diseases #MMPMID28401333
  • Spires-Jones TL ; Attems J ; Thal DR
  • Acta Neuropathol 2017[Aug]; 134 (2 ): 187-205 PMID28401333 show ga
  • Neurodegenerative diseases such as Alzheimer's disease (AD), frontotemporal lobar degeneration (FTD), Lewy body disease (LBD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) have in common that protein aggregates represent pathological hallmark lesions. Amyloid ?-protein, ?-protein, ?-synuclein, and TDP-43 are the most frequently aggregated proteins in these disorders. Although they are assumed to form disease-characteristic aggregates, such as amyloid plaques and neurofibrillary tangles in AD or Lewy bodies in LBD/PD, they are not restricted to these clinical presentations. They also occur in non-diseased individuals and can co-exist in the same brain without or with a clinical picture of a distinct dementing or movement disorder. In this review, we discuss the co-existence of these pathologies and potential additive effects in the human brain as well as related functional findings on cross-seeding and molecular interactions between these aggregates/proteins. We conclude that there is evidence for interactions at the molecular level as well as for additive effects on brain damage by multiple pathologies occurring in different functionally important neurons. Based upon this information, we hypothesize a cascade of events that may explain general mechanisms in the development of neurodegenerative disorders: (1) distinct lesions are a prerequisite for the development of a distinct disease (e.g., primary age-related tauopathy for AD), (2) disease-specific pathogenic events further trigger the development of a specific disease (e.g., A? aggregation in AD that exaggerate further A? and AD-related ? pathology), (3) the symptomatic disease manifests, and (4) neurodegenerative co-pathologies may be either purely coincidental or (more likely) have influence on the disease development and/or its clinical presentation.
  • |Aging/metabolism/pathology [MESH]
  • |DNA-Binding Proteins/*metabolism [MESH]
  • |Humans [MESH]
  • |Neurodegenerative Diseases/*metabolism/*pathology [MESH]
  • |alpha-Synuclein/*metabolism [MESH]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    Linkout box